Oral glutathione is ineffective in replenishing glutathione levels and reversing the abnormal signaling pathways associated with oxidative stress. Intravenous glutathione has been shown to be effective but is short-lived. N-Acetyl Cysteine, a glutathione precursor, has had limited efficacy in clinical settings and suffers from an adverse effect profile.Null Hypothesis (primary): The administration of FT061452 will not increase serum and intracellular glutathione levels in comparison to N-Acetyl Cysteine (NAC), and placebo.